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DMIC 5001 > Test 4: DTH and Transplant > Flashcards

Test 4: DTH and Transplant Flashcards

1
Q

What is contact dermatitis caused by?

A

CD4+ TH1 cell-mediated hypersensitivity

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2
Q

When is contact dermatitis elicited?

A

Second skin exposure to allergen (first sensitized–>TH1 differentiation)

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3
Q

What are some common dental allergens?

A
  • liquid monomer acrylic
  • proteins in latex
  • accelerators in rubber latex
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4
Q

Are all contact allergens natural proteins?

A

No, some are artificial chemicals and not all proteins

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5
Q

How to contact allergens become immunogenic?

A

-act as haptens attaching to carrier self-protein which is then taken up by Langerhans cells on skin and recognized as foreign particle

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6
Q

What are some characteristics of the inflammatory response from DTH?

A
  • post capillary venules surrounded by lymphocytes
  • blistering and necrosis of epidermal cells
  • pruritic
  • edema
  • infiltrated by basophils and eosinophils
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7
Q

How is the immunological diagnosis determined?

A

Patch Test

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8
Q

How is contact dermatitis treated?

A

Systemic Corticosteroids

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9
Q

What is the major stimulus to transplant rejection?

A

Incompatability of MHC molecules (proteins from MHCs)

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10
Q

What is the difference between Autografts, syngenic grafts, allografts, and xenogenic grafts?

A
  • Auto: from the same person
  • syngenic: from identical twin
  • Allograft: From different person
  • Xenograft: from different species
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11
Q

How many T cells can directly recognize and foreign MHC molecule?

A

2%

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12
Q

When the allogenic MHC molecules are DIRECTLY presented by graft APCs, what cells are stimulated?

A

CD4 and CD8 (nucleated allogenic graft cells have MHC I)

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13
Q

How are allogenic MHC molecules INDIRECTLY presented?

A

Recipient APCs phagocytose remnants of allogenic MHC molecules and present them to CD4 cells

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14
Q

What type of graft rejection is characterized by hemorrhage and thrombotic occlusion, mediated by pre-exisiting Abs in host, and begins within minutes/hours?

A

Hyperacute rejection

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15
Q

What is the major obstacle of xenografts?

A

Natural antibodies to other species’ cells

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16
Q

What two things are tested before transplants?

A

ABO incompatability and Abs against allogenic MHCs

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17
Q

Which T cell is more important in Acute rejection and why?

A

CD8+, epithelial cells from vascularized grafts present MHC I molecules–>vascular and parenchymal injury and necrosis

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18
Q

What is the major cause of graft rejection?

A

Chronic rejection , months to years later (used to be acute, but immunosuppressant drugs helped)

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19
Q

In chronic rejection, what causes the arteriosclerosis in graft tissue?

A

Proliferation of intimal smooth muscle cells

20
Q

What causes the Smooth muscle cell growth?

A

lymphocytes activate macrophages (IFN-gamma) which secrete smooth muscle cell growth factor

21
Q

What causes fibrosis of the graft in chronic rejection?

A

Macrophages secrete mesenchymal cell growth factors–>fibroblasts and collagen

22
Q

Which MHC loci are important for transplant matching?

A

HLA-A and HLA-B, HLA-DR most important

23
Q

What is the highest number of molecule matches that still predict poor survival?

A

4

24
Q

In two-way mixed lymphocyte reaction (MLR), what is the indicator that the lymphocytes are incompatible?

A

radio-labeled DNA used for clonal expansion–>DNA synthesis by both

25
Q

How is One-way MLR different from Two-way?

A

One set of leukocytes is blocked from synthesizing DNA

26
Q

What is used for the low resolution Lymphocytotoxicity test?

A

Anti-sera from a woman that has many pregnancies (expresses many different Abs) that will kill cells if they have the same HLA specificity

27
Q

What does Molecular HLA typing detect?

A

polymorphic nucleotide sequences

28
Q

What is the most important immunosuppressive drug and what is its major action?

A

Cyclosporin: inhibits transcription of genes for cytokines (IL-2 which causes proliferation of T cells)

29
Q

What does TGF-beta do?

A

-generalized immunosuppressive cytokine

30
Q

What is the major drawback of cyclosporin?

A

Renal toxicity (also gingival hyperplasia)

31
Q

What can be used as a substitute for Cyclosporin?

A

FK506=Tacrolimus; less renal toxicity

32
Q

What drug has a synergistic effect with cyclosporin?

A

Rapamycin/Sirolimus (inhibits a kinase involved in IL-2 signalling)

33
Q

What makes Mycophenolate Mofetil lymphocyte specific?

A

It blocks de novo synthesis of purines: lymphocytes rely on this more than other cells

34
Q

Immunological effects of corticosteroids

A
  • reduced number of MHC II molecules
  • inhibit T cell activation
  • inhibit T cell migration and release of IFN-gamma (macrophage activation)
35
Q

How do corticosteroids affect inflammation?

A
  • stops cytokine and NO
  • reduces emigration of lymphocytes
  • induces apoptosis of lymphocytes and eosinophils
36
Q

What are two commonlyused corticosteroids?

A

Prednisone and methyl-prednisone

37
Q

What is the most commonly transplanted tissue? Organ?

A

Tissue=cornea

Organ=kidney

38
Q

How long do recipients of kidney transplants have to be on immunosupressive therapy?

A

Their whole lives

39
Q

Why is immunosuppressive therapy needed even with an identical twin donor?

A

subtle differences in minor histocompatability immunogens

40
Q

When would you need a bone marrow transplant?

A

SCID, Aplastic anemia, Leukemia and anemia

41
Q

Where do the donor stem cells come from?

A
  • iliac crest

- peripheral stem cells

42
Q

What does the recipient need to have done before receiving a bone marrow transplant?

A

ablation of all lymphocytes

43
Q

How can you tell that a bone marrow transplant was successful?

A

peripheral leukocytes and mature PMNs in a few weeks

44
Q

What happens in Graft Vs Host Disease (GVHD)?

A

Graft cells recognize the recipient cells as foreign (can be good with leukemia–will attack those cells)

45
Q

Where can GVHD be manifested?

A

Skin and mucous membranes
Liver
Small intestinal epithelia

DMIC 5001 (15 decks)

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